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Biomedical subjects

H A Gross

Publications and source records attributed to H A Gross.

13 recordsLinked to original sources
PubMed1981

Effect of bethanechol on gastric functions in primary anorexia nervosa.

We have shown previously that patients with primary anorexia nervosa (PAN) have decreased gastric emptying and acid output. The present studies were designed to explore the possibility that bethanechol, a parasympathomimetic agent, would acutely restore normal gastric function in those patients. We used a dye dilution technique to determine acid output and fractional emptying rate in 5 patients with PAN and 11 healthy controls during a basal period and following bethanechol (0.06 mg/kg, subcutaneously). Although bethanechol caused fractional emptying and acid output to increase threefold in PAN (P less than 0.05), it failed to produce stimulation of gastric emptying and acid output to levels similar to those achieved in controls. Therefore, gastric emptying and acid output were less in PAN than in controls, both basally and after bethanechol. Since bethanechol failed to completely restore acute gastric function, the defect of emptying and acid output in PAN does not appear to be caused by a deficiency of parasympathetic neurotransmitter but, instead, could reflect undetermined inhibitory influences or impaired function of the muscular and glandular cells. Following weight gain, fractional emptying rate and acid output were still slightly less in PAN patients than in controls, but the difference was statistically significant only for basal acid output.

Adolescent↗
PubMed1981

A double-blind controlled trial of lithium carbonate primary anorexia nervosa.

In this 4-week, double-blind, parallel group study, eight young women with primary anorexia nervosa were evaluated on lithium carbonate, and eight patients were treated with placebo and served as a control. All patients participated in a behavior modification treatment program. The lithium-treated and placebo groups were comparable on nearly all findings measured at baseline (t tests), with no significant differences observed except for calories per day, percent fat composition of the daily calories, "interpersonal sensitivity" on the Hopkins Symptom Checklist-90 (HSCL-90), "self-care" on the Goldberg Anorectic Attitude Questionnaires, (GAAQ) and "manipulation of others" on the physician-rated Psychiatric Rating Scale (PRS). The data were analyzed using repeated measures analysis of covariance (ANCOVA) with the baseline measure as the covariate. Group differences appeared in the areas of "denial or minimization of illness" on the GAAQ, "selective appetite" on the PRS, and weight. Although the repeated measures ANCOVA for weight revealed a significant group-by-time interaction, indicating nonparallelism and invalidating the test for group differences, ANCOVAs performed for each individual time point showed greater weight gain in the lithium group at weeks 3 and 4.

Adolescent↗
PubMed1979

Increased insulin binding to erythrocytes in anorexia nervosa: restoration to normal with refeeding.

We studied [125I] insulin binding to circulating cells in patients with anorexia nervosa (eight females), in the basal cachectic state (seven patients) and after weight gain (eight patients) and compared the values to those obtained in 17 normal volunteers (eight females and nine males). Untreated patients showed increased insulin binding to receptors on erythrocytes (mean +/- S.E.M., 12.2 +/- 0.99 per cent of total); after weight gain, these increased levels returned to normal (6.8 +/- 0.42 vs 6.7 +/- 0.63 per cent of total). Increased binding was due to an increased number of receptors per cell, with little or no change in receptor affinity. In five patients (one untreated, four treated), results of [125I] insulin binding to erythrocytes correlated closely (r = 0.982) with results obtained with monocytes. We conclude that in patients with anorexia nervosa, insulin binding to receptors is altered and that the abnormality is corrected by restoration of normal food intake and body weight.

Adolescent↗
PubMed1979

Catecholamine metabolism in primary anorexia nervosa.

Abnormalities in neuroendocrine function and sympathetic nervous system activity appear to be present in primary anorexia nervosa. Hypothalamic catecholamines are involved in control of endocrine function and norepinephrine is released from sympathetic nerve endings. Because of possible abnormalities in catecholamine metabolism, plasma levels of norepinephrine and urinary excretion of homovanillic acid and 3-methoxy-4-hydroxyphenyl glycol were studied in female patients with primary anorexia nervosa before and after significant clinical improvement and compared with normal female volunteers. During the phase of the disease in which body weights were more than 20--25% below ideal, patients' blood pressures and pulse rates, plasma levels of norepinephrine, and 24-h urinary excretion of 3-methoxy-4-hydroxyphenol glycol and homovanillic acid were lower than those of a group of normal volunteers. After weight gain, these parameters increased to near-normal levels. At no time was plasma dopamine-beta-hydroxylase activity abnormal. The results suggest that abnormalities in catecholamine metabolism in primary anorexia nervosa are caused by starvation, and that neuronal functions dependent on aminergic neurotransmission may be altered as a result.

Adolescent↗
PubMed1979

Altered gastric emptying and secretion in primary anorexia nervosa.

Primary anorexia nervosa (PAN) is an important psychiatric disease with a 7--21% mortality rate. Although altered gastrointestinal function may be an important aspect of its pathophysiology, no information is available concerning gastric emptying and secretion in those patients. During fasting, fractional emptying rates and hydrogen ion (H+) output were decreased twofold in PAN, as compared with healthy controls, and fluid output was slightly but not significantly decreased. Pentagastrin-induced peak stimulation of H+ output in PAN was 64% of that found in controls (P less than 0.05). Peak gastric fluid output was also significantly less in PAN patients, but suppression of fractional emptying produced by pentagastrin was of the same magnitude in both groups. Following a 250-ml water load, the magnitude and the duration of both the emptying and secretory responses were less in PAN patients than in controls. As a result, the initial increase of intragastric volume was greater in PAN patients than in controls, and the gradual return to fasting volume was delayed in those patients. Follow weight gain, fractional emptying tended to return toward control values, but was still significantly less than in controls following the water load. Gastric H+ and fluid output were not significantly modified following weight gain.

Adult↗
PubMed1978

Effects of self-induced starvation on cardiac size and function in anorexia nervosa.

Cardiac size, function and rhythm were examined in 11 patients with anorexia nervosa. Mean left ventricular, left atrial and aortic dimensions on echocardiogram were below normal adult values at baseline. In addition to decreased cardiac dimensions--ventricular ectopy, relative hypotension, bradycardia and blunted heart rate--response to exercise were noted. Left ventricular systolic function, however, was unimpaired as indicated by normal echocardiographic fractional shortening, and by normal exercise augmentation of ejection fraction determined by radionuclide cineangiography. Eight of the patients responded to treatment with a mean weight gain of 32%. In these eight, cardiac dimensions increased toward normal: left ventricular dimension increased by 13%; left atrial dimension by 20%; aortic dimension by 15% and estimated left ventricular mass by 20%. We conclude that abnormalities of heart size and rhythm occur in patients with anorexia nervosa. However, cardiac dimensions, including left ventricular mass, may increase following nutritional rehabilitation, accompanied by an increase in heart rate and blood pressure.

Adolescent↗
PubMed1977

Prostaglandins. A review of neurophysiology and psychiatric implications.

This article reviews the function of prostaglandins (PGs) in the nervous system and discusses the possible alterations in PG metabolism as relating to mental illness. The PGs are a unique group of cyclic fatty acids whose immediate precursors are thought to function postsynaptically by inhibition or facillitation of neurotransmission through cyclase inhibition or activation, and by means of a negative feedback loop to inhibit further release of neurotransmitter from the presynaptic nerve. A review of PGs in psychiatric conditions is presented as well as a discussion of the interaction of psychoactive drugs with the PGs. The concluding section of this review discusses possible future strategies to provide insight into PG physiology as it relates to synaptic transmission in normal and pathological conditions in man.

Central Nervous System↗
PubMed1977

Prostaglandin F in patients with primary affective disorder.

Two aspects of prostaglandin F (PGF) metabolism were assessed in patients with primary affective disorder. For a group of hospitalized patients cerebrospinal fluid PGF was measured by radioimmunoassay and the effects of probenecid and L-tryptophan were determined. For outpatients attending our Lithium Clinic, plasma PGF was measured and the acute and chronic effects of lithium were determined. The results of the studies reveal apparently normal concentrations of PGF in cerebrospinal fluid. These concentrations increase twofold after probenecid, indicating that PGF is transported out of the central nervous system by a probenecid-sensitive active transport system. Evidence for inhibition of PGF synthesis during L-tryptophan treatment was found. The results for outpatient plasma studies suggest no effect on PGF with 12 weeks of lithium treatment, although a slight elevation of plasma PGF with chronic lithium treatment may occur. Specificity of the assay technique as applied to plasma is discussed. This is the first report of the direct measurement of PGF in a psychiatric disorder.

Adult↗